Thomas First Aid Cardio Pharm

Front 1

4 classes of drugs used to treat HTN

Back 1

ACE inhibitors
ARBs
diuretics
Ca-channel blockers

Front 2

Hydralizine
mech
1st line therapy
coadministered with
contraindications

Back 2

increased cGMP to vasodilate arterioles and decrease BP (decreases afterload). HydrAlAzine= vAsodilates Arterioles
1st line- pregnant HTN (with methyldopa)
coadministered- with beta blockers to prevent reflex tachycardia
contraindication- angina/CAD (can cause reflex tachycardia)

Front 3

hydralizine toxcities (4)

Back 3

SLE-like syndrome
reflex tachycardia
fluid retention
angina

Front 4

Nifidepine, Verapamil, Diltiazem
drug class?
affect smooth muscle and cardiac muscle differently, which choice for smooth muscle relaxation? cardiac?
Toxicities (3)

Back 4

Ca-channel blockers
Nifedipine = smooth muscle relaxation (similar to Calcium channel blocker effects)
Verapamil= cardiac depression (Verapamil = ventricle, similar to beta blocker effects)
toxicities- AV block and cardiac depression, hypotension (dizziness, edema), constipation

Front 5

nitrates mechanism and indications (2). toxicites (3)

Back 5

cause increased NO release, increase cGMP, dilate venous smooth muscle (which decreases preload)
indications= angina, pulmonary edema
toxicities= reflex tachycardia, dizziness, headache

Front 6

pt that gets tachycardia, headache, dizziness on mondays when goes to work in industrial plant, what is problem

Back 6

works making nitroglycerin, tolerance over week but lost on weekend

Front 7

Nitroprusside, Fenoldopam, and Diazoxide treatment for?
2 toxicities associated

Back 7

malignant HTN
Nitroprusside releases cGMP but can cause cyanide toxicity
Fenoldopam is D1 agonist- increases renal blood flow
Diazoxide- K+ channel opener, so relaxes smooth muscle but can cause hyperglycemia

Front 8

Fenoldopam action

Back 8

D1 receptor agonist - relaxes renal vascular smooth muscle

Front 9

of following variables, what two do Nitrates increase? Beta blockers? (2 each)
EDV
BP
CTY
HR
Ejection Time
02 consumption

Back 9

Nitrates- increase CTY, HR (both reflex mechanisms)
Beta blockers- increase Ejection time, EDV

Front 10

which class of beta blockers are contraindicated in angina

Back 10

partial agonists (pindolol, acebutalol)

Front 11

What is lipid-lowering agent of choice for:
decreasing LDL
increasing HDL
decreasing TGs

Back 11

decreasing LDL- Statins
increasing HDL- Niacin
decreasing TGs- Fibrates

Front 12

Statin mech, toxicities (2)

Back 12

inhibit mevalonate (cholesterol precursor)
hepatotoxicity, rhabdomyolysis (worsened with coadministration of Fibrates)

Front 13

Niacin mech, toxicities (3)

Back 13

reduces hepatic VLDL secretion into circulation
toxicities- flushing (dec. with aspirin), hyperglycemia, hyperuricemia

Front 14

which lipid-lowering drug can cause hyperuricemia?

Back 14

niacin

Front 15

which lipid lowering drugs can cause cholesterol gallstones

Back 15

Cholestyramine (Bile Acid resins), fibrates

Front 16

lipid-lowering drug patients hate because it tastes bad, causes GI distress, steatorrhea, cholesterol gallstones

Back 16

Cholestyramine (bile acid resins)

Front 17

Ezetimibe
mech
toxicity

Back 17

decreases LDL by inhibitng choleterol absorption
toxicity - rare increase in LFTs

Front 18

Fibrate mech, 4 toxicities

Back 18

upregulate LPL (highly decrease TGs)
toxicities- myositis (especially with statins), hyperuricemia, hepatotoxicity, cholesterol gallstones

Front 19

location of L-type ca channels vs. ryanodine receptor calcium channels

Back 19

both coupled together, L-type is voltage gated on plasma membrane surface (for Ca into cytoplasm), ryanodine is on sarcoplasmic reticulum (which is ca channel also increasing cytoplasmic ca)

Front 20

B1 receptor stimulation in cardiac myosites stimulate Gs--> PKA--> phosphorylation of what

Back 20

L-type voltage-gates ca channels (same channels blocked by beta blockers and ca channel blockers)

Front 21

digoxin clinical uses (2), stimulates what nerve?

Back 21

CHF (b/c increase CTY), afib (depresses SA and AV nodes)
stimulates vagus nerve

Front 22

2 types of toxicity for digoxin, 3 conditions that make it worse

Back 22

cholinergic - n/v, dizziness, blurry yellow vision (Van Gogh would take digitalis cuz he's crazy)
ECG- increased PR t-wave inversion, hyperkalemia
worsening conditions- renal impairment (renally excreted), hypokalemia (easier for digoxin to bind to K+ site on Na/K ATPase), quinidine (displaces it from tissue-binding sites)

Front 23

hyperkalemia, t-wave inversion, increased PR indicate?
tx

Back 23

digoxin overdose
normalize K+, Mg2+, lidocaine, anti-dig Fab

Front 24

Class IA, IB, IC are what anti-arrhythmic drug class? which best for reentrant atrial or ventricular arrhythmias? Post-MI arrhythmias?

Back 24

Na+ channel blockers
reentrant (SVT, vtach) - IA
post MI arrhythmia- IB

Front 25

3 class IA drugs

Back 25

Quinidine
Procainamide
Disopyramide

Front 26

Quinidine class and 3 toxcities

Back 26

IA
thrombocytopenia
torsades de pointes (inc. QT)
cinchonism

Front 27

Procainamide class and side effect

Back 27

IA
SLE-like syndrome

Front 28

3 class IB drugs

Back 28

Lidocaine
Mexiletine
Tocainide

Front 29

what state causes increased toxicity for all Na channel blockers

Back 29

hyperkalemia

Front 30

Beta blockers: class II
affect what second messenger system, what phase of nodal AP?

Back 30

decrease cAMP, decrease phase 4 (inhibit ca channel currents)

Front 31

3 clinical antiarrhythmic uses of beta blockers

Back 31

SVT, V-tach, decrease ventricular rate in afib/flutter (because AV very sensitive to beta blockers)

Front 32

beta blockers can mask signs of?
treat overdose of beta blockers with?

Back 32

hypoglycemia
glucagon

Front 33

metoprolol-specific toxicity

Back 33

can cause dyslipidemia

Front 34

Dofetilide

Back 34

class III antiarrhythmic (K+ channel blocker)

Front 35

Bretylium class and toxicities (2)

Back 35

class III antiarrhythmic (K+ channel blocker)
hypotension, arrhythmias

Front 36

Ibutilide class and toxicity

Back 36

class III antiarrhythmic (K+ channel blocker)
torsades de pointes

Front 37

amiodarone class and toxicities (5)

Back 37

class III antiarrhythmic (K+ channel blocker)
pulmonary fibrosis, photosensitivity, hypothyroidism/hyperthyroidism (40% iodine by weight)
hepatotoxicity
heart block

Front 38

amiodarone has class I,II,III,IV antiarrhythmic effects because

Back 38

it alters lipid membranes

Front 39

two class IV antiarrhythmics, indication, 2 types of toxicity

Back 39

ca++ channel blockers
verapamil, diltiazem
prevent nodal arrhythmias (SVT, etc)
flushing/constipation/edema, CV effects (CHF, AV block)

Front 40

Adenosine action, indication, drug that blocks

Back 40

increases K+ release out of cells
1st line for SVT
blocked by theophylline

Front 41

2 indications for Mg2+

Back 41

digoxin toxicity, torsades de pointes

Front 42

K+ indication

Back 42

digoxin toxicity (hypokalemia arrhythmias)